Beta-hydroxy beta-methyl butyrate decreases muscle protein degradation via increased Akt/FoxO3a signaling and mitochondrial biogenesis in weanling piglets after lipopolysaccharide challenge

Beta-hydroxy beta-methyl butyrate decreases muscle protein degradation via increased Akt/FoxO3a signaling and mitochondrial biogenesis in weanling piglets after lipopolysaccharide challenge
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脂多糖攻击后,β-羟基β-甲基丁酸酯通过增加 Akt/FoxO3a 信号传导和线粒体生物发生来减少断奶仔猪的肌肉蛋白降解

DOI:
10.1039/c9fo00769e
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发表时间:
2019-08-01
期刊:
影响因子:
6.1
通讯作者:
Yin, Yutong
Yin, Yutong
中科院分区:
农林科学1区
文献类型:
--
作者:
Duan, Yehui;Zheng, Changbing;Yin, Yutong

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本研究的目的是研究膳食β-羟基-β-甲基丁酸(HMB)对脂多糖(LPS)诱导的肌肉萎缩的影响,并探讨其机制。在2 × 3析因设计中使用60头猪(21 +/- 2日龄,5.86 +/- 0.18 kg体重),主要因素包括饲料(0、0.60%或1.20% HMB)和免疫激发(LPS或盐水)。用LPS和/或HMB处理15 d后,测量生长性能、血液参数和肌肉蛋白降解率。结果表明,添加0.60% HMB可显著提高注射LPS猪的平均日增重和平均日采食量,降低料重比(P < 0.05),提高瘦肉率。添加0.60%HMB可显著降低血清尿素氮、IL-1 β和TNF-α浓度以及肌肉蛋白降解率和细胞凋亡率(P < 0.05)。此外,饮食HMB补充(0.60%)调节参与线粒体生物发生的基因的表达,并增加选定肌肉中Akt和Forkhead Box O3 a(FoxO 3a)的磷酸化,伴随着肌肉RING finger 1和肌肉萎缩F-box的蛋白表达降低。这些结果表明,HMB可以发挥保护作用,对LPS诱导的肌肉萎缩,通过正常化Akt/FoxO 3a轴,调节泛素蛋白水解和改善线粒体生物合成。
The aim of this study was to investigate the effects of dietary beta-hydroxy-beta-methylbutyrate (HMB) on lipopolysaccharide (LPS)-induced muscle atrophy and to investigate the mechanisms involved. Sixty pigs (21 +/- 2 days old, 5.86 +/- 0.18 kg body weight) were used in a 2 x 3 factorial design and the main factors included diet (0, 0.60%, or 1.20% HMB) and immunological challenge (LPS or saline). After 15 d of treatment with LPS and/or HMB, growth performance, blood parameters, and muscle protein degradation rate were measured. The results showed that in LPS-injected pigs, 0.60% HMB supplementation increased the average daily gain and average daily feed intake and decreased the feed : gain ratio (P < 0.05), with a concurrent increase of lean percentage. Moreover, 0.60% HMB supplementation decreased the serum concentrations of blood urea nitrogen, IL-1 beta, and TNF-alpha and the rate of protein degradation as well as cell apoptosis in selected muscles (P < 0.05). In addition, dietary HMB supplementation (0.60%) regulated the expression of genes involved in mitochondrial biogenesis and increased the phosphorylation of Akt and Forkhead Box O3a (FoxO3a) in selected muscles, accompanied by decreased protein expression of muscle RING finger 1 and muscle atrophy F-box. These results indicate that HMB may exert protective effects against LPS-induced muscle atrophy by normalizing the Akt/FoxO3a axis that regulates ubiquitin proteolysis and by improving mitochondrial biogenesis.